نتایج جستجو برای: 1 antitrypsin a1at

تعداد نتایج: 2753541  

1999
Ping Yang Kimberly A. Wentzlaff Jerry A. Katzmann Randolph S. Marks Mark S. Allen Timothy G. Lesnick Noralane M. Lindor Jeffrey L. Myers Elaine Wiegert David E. Midthun Stephen N. Thibodeau Michael J. Krowka

Lung cancer (LC) and chronic obstructive pulmonary lung diseases (COPDs; including emphysema and chronic bronchitis) share a common etiology. Despite the known associations of alpha1-antitrypsin deficiency (a1AD) with COPD and COPD with LC, few studies examined the association of a1AD alleles and LC. We hypothesize that heterozygous individuals who carry a deficient allele of the a1AD gene Pi (...

Journal: :Respiratory care 2014
James K Stoller Charlie Strange Laura Schwarz Thomas J Kallstrom Robert L Chatburn

BACKGROUND Alpha-1 antitrypsin deficiency is under-recognized. We hypothesized that respiratory therapists (RTs) could help improve the detection rate of individuals with alpha-1 antitrypsin deficiency. The American Association for Respiratory Care (AARC) and Alpha-1 Foundation recently collaborated to create an online alpha-1 antitrypsin deficiency training program for RTs. This study aimed to...

Journal: :iranian journal of allergy, asthma and immunology 0
mohammad r. fazlollahi asghar aghamohammadi reza farid abbas s. lotfi alireza khoshdel abolhassan farhoudi

primary antibody deficiencies are the most frequent primary immunodeficiency disorders. bronchiectasis as a feature of these disorders may be developed due to some factors such α-1-antitrypsin deficiency. in order to determine the prevalence of two common α-1-antitrypsin deficiency alleles (pi*z and pi*s) in iranian patients with antibody deficiency, this study was performed. the prevalence of ...

2011
James K Stoller Helen Hollingsworth

INTRODUCTION — Alpha-1 antitrypsin (AAT) deficiency is a clinically underrecognized inherited disorder affecting the lung, liver, and rarely skin. The characteristics of the pulmonary manifestations of this disorder will be reviewed here [1-4]. Extrapulmonary disease and therapy are discussed separately. (See "Extrapulmonary manifestations of alpha-1 antitrypsin deficiency" and "Treatment of al...

2014
A. Dickens Dawn L. DeMeo Juan Perez S. Tamir Rashid James Day Adriana Ordoñez J. Marciniak Imran Haq Alan F. Barker Edward J. Campbell Edward Eden Noel G. McElvaney Stephen I. Rennard Robert A. Sandhaus James M. Stocks James K. Stoller Charlie Strange Gerard Turino Farshid N. Rouhani Mark Brantly David A. Lomas

Most individuals carry two wild-type M alleles of the SERPINA1 gene which encodes a1-antitrypsin. 95% of severe deficiency of a1-antitrypsin is associated with the Z allele (Glu342Lys; denoted PiZZ in the homozygote), and with the retention and polymerisation of a1-antitrypsin within hepatocytes [1]. These polymers are contained within periodic acid–Schiff-positive, diastase-resistant inclusion...

Journal: :The Journal of clinical investigation 1975
G N Olsen J O Harris J R Castle R H Waldman H J Karmgard

The content of alpha-1-antitrypsin in the serum, alveolar lavage fluid, and alveolar macrophages of smokers and nonsmokers was studied. Bronchoalveolar lavage was used to obtain alveolar fluid and macrophages from normal volunteers, and alpha-1-antitrypsin and albumin were measured using the electroimmunodiffusion technique. The serum level of inhibitor was not different between the two groups,...

Journal: :The Journal of clinical investigation 1973
A B Cohen

Alveolar macrophages lavaged from human lungs contain protease activity at an optimum pH of 3.0 and possibly a lesser peak of activity at pH 5.5. Protease activity measured at pH 4.1 is inhibited by purified alpha-1-antitrypsin. Fluorescent antibody studies of human alveolar macrophages showed that alpha-1-antitrypsin is present in normal alveolar macrophages. In addition, macrophages from a pa...

Journal: :Thorax 2011
Jennifer K Quint Gavin C Donaldson Meena Kumari Philippa J Talmud John R Hurst

BACKGROUND The α(1)-antitrypsin 11478G→A polymorphism may be associated with attenuated acute α(1)-antitrypsin responses. It was hypothesised that patients with chronic obstructive pulmonary disease (COPD) and this mutation have accelerated lung function decline. OBJECTIVE To assess whether the 11478G→A polymorphism is associated with attenuated α(1)-antitrypsin responses at COPD exacerbation...

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